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PubMed1993

Immunogenetic analysis of silicosis in Japan.

We previously reported that a gene in linkage disequilibrium with HLA-Bw54, DR4, and DRw53 might control the susceptibility to silicosis (K. Honda et al. 1988. N. Engl. J. Med. 319:1610). To further define the HLA-linked gene and other genetic factors for predisposition of silicosis, we determined for HLA-DQ and DP alleles using the polymerase chain reaction and sequence-specific oligonucleotide probes and made a restriction fragment length polymorphism (RFLP) analysis of the fourth component of complement (C4) genes, immunoglobulin lambda variable chain (IGLV) gene, and T-cell receptor alpha and beta genes in 46 Japanese patients with silicosis. The frequency of DQB1*0401 (relative risk [RR] = 2.2, P < 0.02) was increased and that of DQB1*0601 (RR = 0.36, P < 0.01) was decreased in the patients. RFLP analysis of C4 and IGLV genes showed significant association between silicosis and a specific RFLP pattern of C4A3-C4B5 allotype (RR = 2.3, P < 0.05) and that of IGLV 5.3 kb (RR = 0.33, P < 0.003). No other genetic markers showed significant association. Statistical analyses of the associated genetic markers revealed that the HLA-Bw54 was the allele that showed primary association with silicosis and the frequencies of the C4 and HLA-DQ alleles were suggested to be increased due to their linkage disequilibrium with the HLA-Bw54. We conclude that the major gene for silicosis may be mapped near the HLA-B locus.

Adolescent↗
PubMed2004

A biphasic response to silica: I. Immunostimulation is restricted to the early stage of silicosis in lewis rats.

Inhalation of crystalline silica may lead to acute or chronic silicosis. Although chronic silicosis is associated with increased incidence/exacerbation of autoimmune disorders, the immunologic effects of chronic silicosis are not completely understood. In an animal model of chronic silicosis, Lewis rats were exposed to filtered air or silica (1.75 microm average particle size) at an exposure concentration of 6.2 mg/m(3), 6 h/d, 5 d/wk for 6 wk, and observed up to 27 wk after the exposure. Based on silica burden, lung histopathology, and immunologic changes, two distinct stages were identified in the development of chronic silicosis. Stage 1 (4-28 d after exposure) was characterized by silica deposition in various tissues, and augmented antibody and cellular immunity. Although bronchoalveolar lavage contained an increased number of activated macrophages, protein and lactate dehydrogenase levels were comparable to controls. In Stage 2 (>/= 10 wk), silica was localized in epithelioid macrophages, and T cell immunity had returned to normal, but the lavage fluids contained increased protein concentration and lactate dehydrogenase activity. Moreover, lungs from silica-treated animals contained neutrophils and lymphocytes, and exhibited granulomatous changes around the silica-containing epithelioid macrophages. Thus, in the early stages of silicosis, silica activates the immune system; however, the progression of lung granulomas does not depend on a continually activated adaptive immune system.

Animals↗
PubMed2006

Alterations of Fas and Fas-related molecules in patients with silicosis.

Persons with silicosis have not only respiratory disorders but also autoimmune diseases. To clarify the mechanisms involved in the dysregulation of autoimmunity found in patients with silicosis, we have been focusing on Fas and Fas-related molecules in the Fas-mediated apoptotic pathway, because Fas is one of the most important molecules regulating auto-immunity involving T cells. Our findings showed that patients with silicosis exhibited elevated serum soluble Fas levels, an increased relative expression of the soluble fas and dcr3 genes in peripheral blood mononuclear cells, high levels of other variant messages of the fas transcript, relatively decreased expression of genes encoding several physiological inhibitors (such as survivin and toso), and dominancy of lower-membrane Fas expressers in lymphocytes, which transcribe soluble fas dominantly, compared with soluble fas transcription in healthy donors. These findings are consistent with known features regarding immunological factors, such as serum immunogulobulin G levels and the titer of anti-nuclear autoantibodies in silicosis. In addition, anti-caspase 8 autoantibody and anti-Fas autoantibody were detected in serum specimens from patients with silicosis, and a functional assay showed that anti-Fas antibody stimulated Fas-mediated apoptosis. We hypothesize that there are two subpopulations of silicosis lymphocytes. One is a long-term surviving fraction that includes self-recognizing clones showing lower levels of membrane Fas and inhibition of Fas/Fas ligand binding in extracellular spaces. The other subpopulation exhibits apoptosis caused by silica and silicates, is recruited from bone marrow, shows higher levels of membrane Fas, and is sensitive to anti-Fas autoantibody. Further investigation should be performed to confirm the effects of silica and silicates on the human immune system.

Autoantibodies↗
PubMed2004

Highway repair: a new silicosis threat.

OBJECTIVES: We describe an emerging public health concern regarding silicosis in the fast-growing highway repair industry. METHODS: We examined highway construction trends, silicosis surveillance case data, and environmental exposure data to evaluate the risk of silicosis among highway repair workers. We reviewed silicosis case data from the construction industry in 3 states that have silicosis registries, and we conducted environmental monitoring for silica at highway repair work sites. RESULTS: Our findings indicate that a large population of highway workers is at risk of developing silicosis from exposure to crystalline silica. CONCLUSIONS: Exposure control methods, medical screenings, protective health standards, and safety-related contract language are necessary for preventing future occupational disease problems among highway repair workers.

Air Pollutants, Occupational↗
PubMed1986

Silicosis in a grey iron foundry. The persistence of an ancient disease.

An industrial hygiene and medical survey was conducted in an iron foundry to study the occurrence of silicosis. Breathing zone exposures to respirable crystalline silica had been very high in 1977 [1 045 micrograms/m3 (geometric mean) for coremakers and 198 micrograms/m3 for fettlers]; exposures in 1980 and 1982 were substantially lower. A radiographic evaluation of 188 workers revealed silicosis in 18 (9.6%). Eight had category 1 profusion of small rounded pulmonary lesions (by the 1980 classification of the International Labour Office); two had category 2; and eight had category 3. Two had progressive massive fibrosis. Four workers without silicosis in 1977 had developed lesions by 1980. The prevalence increased from 1.5% among workers employed less than 20 years to 53% among longer term workers. No association was found between the prevalence of silicosis and cigarette smoking. Chronic cough was more common in workers with heavy current dust exposure than in those with light exposure, more common in smokers than in nonsmokers, and more common in silicotics than in nonsilicotics. A multiplicative interaction existed between dust exposure and smoking in the etiology of cough. Silicosis continues to exist in American foundries. Cigarette smoking does not contribute to the causation of silicosis, but it aggravates the attendant respiratory symptoms.

Adult↗
PubMed2002

Silicosis and end-stage renal disease.

OBJECTIVES: The objective of this study was to determine the incidence of renal disease among workers with silicosis. METHODS: A population of 1,328 workers with definite silicosis and adequate work history information, drawn from three states with silicosis surveillance systems, was followed. Renal disease was ascertained via linkage of the cohort with a United States register (which has existed since 1977) of end-stage renal disease. RESULTS: In the first analysis, it was assumed that the risk of end-stage renal disease began upon exposure to silica. In this analysis 12 cases of end-stage renal disease were found versus 15.6 expected, for a rate ratio of 0.77. Four cases of glomerular end-stage renal disease were found (standardized incidence ratio 2.65, 95% confidence interval 0.56-5.25). It is possible that some persons with end-stage renal disease died before being entered into the silicosis registers. In a second analysis, person-time at risk was assumed to begin at the date of entry into the silicosis register. A rate ratio of 1.67 (95% confidence interval 0.76-3.17) was found for end-stage renal disease on the basis of nine observed cases. CONCLUSIONS: The results do not clearly show that patients with silicosis have an excess of end-state renal disease, although they do suggest an excess of glomerular end-stage renal disease. Analyses were limited by small numbers and possible selection biases.

Cohort Studies↗
PubMedDate not supplied

[The dynamics of exposure to silicotic dusts and silicosis in a foundry].

This work presents the concentrations dynamics of dust in a cast iron foundry, in parallel with the frequency and gravity dynamics of the getting sick of silicosis. The knowing of the real risk of exposure to silicotic dust was possible through the data processing concerning the dusting degree (the average of working place), the content of silicon free-crystalline dioxide (SiO2 l.c.) for the calculation of the maximum admitted concentration (C.M.A.) and the dispersion degree of dust in a cast iron and steel foundry for the studied period (1982-1996). New cases of silicosis appeared in this period were studied and they were colligated with the age at declaration, the average length of service and the profession. The values of the dusting degree outrun the C.M.A. up to 168 times, especially at the preparation of mixture and grinding with a prevalence of particles under 3 micron (40-70%) and the Si02 l.c. content varies between 35.2% and 64.5%. From those 98 new cases of silicosis appeared in 15 years, 82.65% were traced out in the incipient phases of the disease. The average age in service and the average age increase (43.1 respective 19.8 years). The coefficients of correlation and regress (+0.286 respective +0.383) show a good correlation between the silicosis number and the age in service. The advanced stages of silicosis and age in service under 10 years were found at the foundry-workers and formators, occupations which imply a high silicotic risk. The foretelling calculations for the next 20 years show an increase of the silicosis incidence for foundry-workers.

Adult↗
PubMed1999

[Hemorrheological status in patients with silicosis and its clinical significance].

OBJECTIVE: To study relationship between silicosis and hemorrheology and its clinical significance. METHODS: Varied indices for hemorrheology were measured in 85 male patients with silicosis, 45 male patients with chronic bronchitis and 100 healthy male subjects. RESULTS: Compared with the control group and the chronic bronchitis patient group, average hematocrit (Hct), whole blood apparent viscosity (eta(a)) at 4 s(-1) - 200 s(-1) shear rates, plasma viscosity (eta(p)), erythrocyte electrophoresis time (EET) and platelet electrophoresis time (PET) all significantly increased in patients with silicosis (P < 0.001). Hemorrheological indices in patients with silicosis increased with severity of disease, increased with decrease in their pulmonary function, and were all significantly higher than those in the control group (P < 0.01 approximately equal 0.001). Stepwise regression analysis showed that severity of disease correlated closely to Hct, eta(a) at 4 s(-1) - 200 s(-1), EET and PET, and that pulmonary function status in patients with silicosis and their courses correlated closely to Hct, eta(a) at 4 s(-1) - 200 s(-1), eta(p), EET and PET. CONCLUSIONS: Blood of patients with silicosis was in highly viscose status, which was easy to be complicated with multiple diseases.

Aged↗
PubMed2002

[The relationship between silicosis and the polymorphism of HLA-DRB1 *, DQB1 * genes].

OBJECTIVE: To investigate the relation between the susceptibility to silicosis and the polymorphism of HLA-DRB1 *, DQB1 * genes in Chinese Hans. METHODS: HLA-DRB1 * and DQB1 * gene polymorphism were tested in 48 silicosis patients and 100 normal controls by using polymerase chain reaction of sequence-specific primers (PCR-SSP). RESULTS: The allele frequencies of DRB1 * 1401 and DQB1 * 05 in silicosis patients were significantly higher than those in normal controls (chi 2 = 5.61, P = 0.0066, RR = 17.40; chi 2 = 10.70, P = 0.0011, RR = 3.81, respectively), while the allele frequency of DRB1 * 09 was significantly lower in silicosis patients than that in controls (chi 2 = 5.70, P = 0.0187, RR = 0.21). There was a significant difference between the patient group and control group. CONCLUSION: HLA-DRB1 * 1401 and DQB1 * 05 may be the susceptible genes and HLA-DRB1 * 09 the protection gene of silicosis, both susceptibility and protection may be related to HLA-DR gene locus. The joint action of allele genes may affect the pathogenesis of silicosis.

Gene Frequency↗
PubMed1976

[Participation of gonads in pulmonary silicosis].

A survey is given on the participation of endocrine glands in the pulmonary silicosis. At the same time a new clinical and experimental contribution to the question of the appearance of a hypogonadotropic hypogonadism is given. The frequency of this hypogonadism increases with the severity of the pulmonary silicosis. The immunological opinions as well as the neuroergonal ones concerning the pathogenesis of pulmonary silicosis gave the possibility of a better explanation of the mechanisms, by means of which also other organs may be attacked in pulmonary silicosis. The neuroendocrine system gives a defensive answer to the aggressive silicotic pulmonary process, which in general slowly progresses, but which may also be certain hormones from the group of the glucocorticosteroids in the adrenal cortex. The intervention into the axis hypothalamus-hypophysis-adrenal cortex has been provided in all defence processes of the organism against every aggression. By the functional or organic damage of the neuroendocrine system, by the immediate toxic effect of silicium dioxide or the monosilicium acid as well as by the effect of the secondary hypoxia in pulmonary silicosis an insufficiency in the stimulation and excretion of certain hormones develops. The origin of this insufficiency is found in the hypothalamo-hypophyseal centres, and the effects extend to all endocrine glands which depend on the system hypothalamus-hypophysis. This mechanism is made responsible for the appearance of a hypogonadotropic insufficiency of gonads in the course of a pulmonary silicosis and is proved clinically and experimentally in the cases investigated by the authors

17-Ketosteroids↗
PubMed1976

[The relation between the morphological stage of silicosis and the SiO2 content in hilar lymph nodes (author's transl)].

There is a positive relation with significant differences in mean values between the severity of silicosis of hilar lymph noeds and their SiO2 contents. The average SiO2 values in silicosis I amount to 2.03 g %; in silicosis II: 2.86 g%, and in silicosis III: 3.89 g%. The average values in exposed miners without silicosis (= 1.70 g%) show no significant differences in comparison with those of silicose I cases and those of nonexposed male persons (= 0.82 g%). The results justify the attempt of a morphological classification of the severity of silicosis in the hilar lymph nodes encouraging the use of chemical examinations of dust for the evaluation of pneumoconioses, for instance, in the material of mediastinoscopies.

Environmental Exposure↗
PubMed1989

[Lung diseases associated with silicosis. Study of 618 cases].

Retrospective research has been carried out on the clinical reports of 618 cases of patients suffering from silicosis admitted to the S. Luigi Gonzaga Hospital in 1973-1987 (1.4% of all pneumopathy admittances). A comparative evaluation of the five-year periods 1973-77, 1978-82, 1983-87 showed a steady reduction in the percentage of silicosis to total cases (from 1.62% to 1.55% and 1.16%). Among the 618 cases assessed, the following pneumopathies were associated with silicosis either alone or in combination: chronic obstructive bronchopneumopathy (89.4%), pulmonary tuberculosis (22.2%), bronchogenic carcinoma (8.4%), acute aspecific infections (26.1%), mycosis (0.6%), sarcoidosis (0.3%), other pneumopathies (1.1%). Comparison between the three five-year periods shows an increase in the frequency of the silicosis-carcinoma association and a fall in the silicosis-tuberculosis and silicosis-COLD associations.

Adult↗
PubMed1995

[The clinical x-ray characteristics and dispensary care of miners with suspected silicosis].

The prospective study covered some principles of silicosis formation in workers of polymetallic mines. Mild and mainly diffuse sclerotic type of silicosis was revealed in 13% of the examinees with suspected silicosis, no additional X-ray data and no history, who were under exposure to the dust during 8-10 years. Variably calcified thoracic lymph nodes prove prominent risk of nodular silicosis (16.7%) and mostly progressive silicotuberculosis (50.0%). Increased vascular markings primarily in lower lungs and history of frequent respiratory infections and repeated pneumonia shows diffuse sclerotic silicosis complicated by chronic bronchitis. The data obtained necessitate further improvement of occupational safety and differentiated treatment and prophylaxis to prevent silicosis with its complications.

Adult↗
PubMed1995

Occupational silicosis--Ohio, 1989-1994.

Silicosis is a chronic lung disease associated with the inhalation and pulmonary deposition of dust that contains crystalline silica. Through the Sentinel Event Notification System for Occupational Risks (SENSOR)* program, CDC's National Institute for Occupational Safety and Health (NIOSH) is assessing practical models for implementing state-based surveillance of silicosis and linking follow-up intervention activities to surveillance reports. From 1989 through 1992, the Ohio Department of Health (ODH) SENSOR program identified silicosis cases through reports of Bureau of Workers' Compensation (BWC) claims, physician reports, and death certificates. The addition in 1993 of hospital discharge reports as an ascertainment source resulted in a substantial increase in the number of silicosis case reports identified annually (Table 1). This report describes the investigation of a case of occupational silicosis in Ohio and summarizes the impact of hospital-based reporting on surveillance for silicosis in Ohio during 1993-1994.

Hospitalization↗
PubMed1993

Silicosis surveillance--Michigan, New Jersey, Ohio, and Wisconsin, 1987-1990.

PROBLEM/CONDITION: Improved surveillance for silicosis is needed to target interventions to prevent this occupational lung disease caused by the inhalation of crystalline silica dust. REPORTING PERIOD COVERED: 1987-1990. DESCRIPTION OF SYSTEMS: State-based silicosis surveillance and intervention programs have been developed in Michigan, New Jersey, Ohio, and Wisconsin as part of the Sentinel Event Notification System for Occupational Risks (SENSOR) Program, initiated in 1987 by the National Institute for Occupational Safety and Health (NIOSH). RESULTS: From 1987 through 1990, the SENSOR program confirmed a total of 430 cases of silicosis reported from these four states. Overall, approximately 60% of these cases were in workers employed in primary metal industries, although the types of industries in which cases occurred varied by state. Some cases were attributable to relatively recent exposure, including new cases in seven persons first exposed since 1980 in New Jersey. Silicosis case reports have prompted measurement of respirable silica concentrations at 25 Michigan work sites, and 14 (56%) of these sites were found to have levels that exceeded the legally permissible exposure level. INTERPRETATION: The silicosis surveillance and intervention strategies piloted by state health departments in the NIOSH-funded SENSOR Program have demonstrated the feasibility and effectiveness of identifying specific silica-using work sites that need preventive intervention. ACTIONS TAKEN: On the basis of initial experience in these four states, NIOSH developed guidelines for state-based silicosis surveillance and awarded SENSOR cooperative agreements to three additional states where the applicability of these surveillance methods will be further evaluated.

Humans↗
PubMed1996

[Clinical evaluation of 201TI single photon emission computed tomography in patients with large opacities due to silicosis with bronchogenic carcinoma].

201T1 single photon emission computed tomography (201T1 SPECT) was used to evaluate 18 patients with large opacities due to silicosis and 22 others with bronchogenic carcinoma. An early scan and a delayed scan were obtained and the retention index was calculated from the early ratio and the delayed ratio. In patients with silicosis, the retention index and the two ratios were significantly lower than in the patients with bronchogenic carcinoma (p < 0.01). In patients with stable shadows on chest X-ray films due to large opacities of silicosis, the delayed ratio was the same as or lower than the early ratio. However, in patients with silicosis who had high activity in large opacities, the delayed ratio was higher than the early ratio. These results suggest that 201)T1 SPECT is useful for evaluating the activity of large opacities in patients with silicosis and for differentiating large opacities caused by silicosis from those caused by bronchogenic carcinoma.

Aged↗
PubMed2000

Is silicosis required for silica-associated lung cancer?

BACKGROUND: Abundant epidemiologic and experimental evidence supports the 1997 International Agency for Research on Cancer classification of crystalline silica as a human lung carcinogen. Nonetheless, there remains uncertainty about whether excessive lung cancer occurs exclusively among workers with silicosis. METHODS: A review was performed of published occupational epidemiologic literature directly pertinent to the interrelations among silica exposure, silicosis, and lung cancer. RESULTS: The association between silica and lung cancer is generally, but not uniformly, stronger among silicotics than nonsilicotics. However, the existing literature is ambiguous due to incomplete or biased ascertainment of silicosis, inadequate exposure assessment, and the inherently strong correlation between silica exposure and silicosis which hinders efforts to disentangle unique contributions to lung cancer risk. CONCLUSIONS: Until more conclusive epidemiologic findings become available, population-based or individually-based risk assessments should treat silicosis and lung cancer as distinct entities whose cause/effect relations are not necessarily linked.

Environmental Exposure↗
PubMed2000

Silica, silicosis, and lung cancer: a risk assessment.

BACKGROUND: To investigate exposure-response relationships for silica, silicosis, and lung cancer. METHODS: Quantitative review of the literature identified in a computerized literature search. RESULTS: The risk of silicosis (ILO category 1/1 or more) following a lifetime of exposure at the current OSHA standard of 0.1 mg/m(3) is likely to be at least 5-10% and lung cancer risk is likely to be increased by 30% or more. The exposure-response relation for silicosis is nonlinear and reduction of dust exposures would have a greater than linear benefit in terms of risk reduction. Available data suggests that 30 years exposure at 0.1 mg/m(3) might lead to a lifetime silicosis risk of about 25%, whereas reduction of the exposure to 0.05 mg/m(3) might reduce the risk to under 5%. CONCLUSIONS: The lifetime risk of silicosis and lung cancer at an exposure level of 0.1 mg/m(3) is high. Lowering exposures to the NIOSH recommended limit if 0.05 mg/m(3) may have substantial benefit.

Adult↗